Han and colleagues discovered that in KRAS mutant pancreatic tumors, fibroblast‐derived NRG1 activated the ERBB2/ERBB3 pathway in tumor cells, enabling them to grow independently of KRAS signaling and leading to resistance against KRAS inhibitors.[83] Following KRAS inhibitor treatment, the expression of ERBB2/3 was significantly increased highlighting the unique role of fibroblasts in conferring resistance to KRAS inhibitors. Here, KRAS is linked to pancreatic neoplasm.